scholarly journals G Protein–Coupled Estrogen Receptor Agonist Improves Cerebral Microvascular Function After Hypoxia/Reoxygenation Injury in Male and Female Rats

Stroke ◽  
2013 ◽  
Vol 44 (3) ◽  
pp. 779-785 ◽  
Author(s):  
Takahiro Murata ◽  
Hans H. Dietrich ◽  
Chuanxi Xiang ◽  
Ralph G. Dacey
Keyword(s):  
Estrogen Receptor ◽  
G Protein ◽  
Receptor Agonist ◽  
Microvascular Function ◽  
Female Rats ◽  
Male And Female ◽  
Male And Female Rats ◽  
Reoxygenation Injury ◽  
G Protein Coupled ◽  
Hypoxia Reoxygenation

scholarly journals GPER1 agonist improves cerebral microvascular function after hypoxia/reoxygenation injury in male and female rats

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Takahiro Murata ◽  
Hans H. Dietrich ◽  
Tetsuyoshi Horiuchi ◽  
Kazuhiro Hongo ◽  
Ralph G. Dacey
Keyword(s):  
Microvascular Function ◽  
Female Rats ◽  
Male And Female ◽  
Male And Female Rats ◽  
Reoxygenation Injury ◽  
Hypoxia Reoxygenation

Endothelium-dependent relaxation by G protein-coupled receptor 30 agonists in rat carotid arteries

2010 ◽  
Vol 298 (3) ◽  
pp. H1055-H1061 ◽  
Author(s):  
Brad R. S. Broughton ◽  
Alyson A. Miller ◽  
Christopher G. Sobey
Keyword(s):  
Nitric Oxide ◽  
G Protein ◽  
Arterial Wall ◽  
Carotid Arteries ◽  
Female Rats ◽  
Sprague Dawley ◽  
G Protein Coupled Receptor ◽  
Male And Female ◽  
Male And Female Rats ◽  
G Protein Coupled

Recent studies have identified that the novel membrane estrogen receptor, G protein-coupled receptor 30 (GPR30), is present in blood vessels. However, the signaling mechanisms associated with GPR30 in the vasculature remain unclear. We examined whether putative agonists of GPR30 exert vasorelaxant and/or antioxidant effects similar to those reported for estrogen. Using wire myography, we assessed the role of the endothelium in relaxation responses to the GPR30 agonists, G-1 and 5408-0877 (1 nM-10 μM), in U-46619-precontracted common carotid arteries from Sprague-Dawley rats. Furthermore, using lucigenin (5 μM)-enhanced chemiluminescence, we tested the effect of G-1 (10 μM) on superoxide levels. Specific immunofluorescence was also used to confirm GPR30 expression in the arterial wall. We found that G-1 and 5408-0877 induced a concentration-dependent relaxation in carotid arteries from both male and female rats. Interestingly, G-1- and 5408-0877-induced relaxation was abolished by endothelium removal and abrogated in the presence of the nitric oxide synthase inhibitor NG-nitro-l-arginine methyl ester (100 μM). In addition, G-1 significantly decreased NADPH (100 μM)-stimulated superoxide production by carotid and intracranial (pooled basilar and middle cerebral) arteries but also attenuated the superoxide signal detected in a cell-free xanthine/xanthine oxidase assay. Furthermore, GPR30 immunoreactivity was observed in endothelial and vascular smooth muscle cells of carotid arteries from both genders. These findings indicate that GPR30 is expressed throughout the arterial wall and that GPR30 agonists elicit endothelial-derived nitric oxide-dependent relaxation of the carotid artery in male and female rats. Additionally, G-1 appears to directly scavenge superoxide anion.

scholarly journals G-Protein-Coupled Estrogen Receptor Agonist Suppresses Airway Inflammation in a Mouse Model of Asthma through IL-10

PLoS ONE ◽  
2015 ◽  
Vol 10 (3) ◽  
pp. e0123210 ◽  
Author(s):  
Masamichi Itoga ◽  
Yasunori Konno ◽  
Yuki Moritoki ◽  
Yukiko Saito ◽  
Wataru Ito ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Mouse Model ◽  
Airway Inflammation ◽  
G Protein ◽  
Receptor Agonist ◽  
G Protein Coupled

scholarly journals Estradiol activates epithelial sodium channels in rat alveolar cells through the G protein-coupled estrogen receptor

2013 ◽  
Vol 305 (11) ◽  
pp. L878-L889 ◽  
Author(s):  
Megan M. Greenlee ◽  
Jeremiah D. Mitzelfelt ◽  
Ling Yu ◽  
Qiang Yue ◽  
Billie Jeanne Duke ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Plasma Membrane ◽  
G Protein ◽  
Sodium Channels ◽  
Female Rats ◽  
Channel Activity ◽  
Alveolar Cells ◽  
Α Subunit ◽  
Female Sex ◽  
G Protein Coupled

Female sex predisposes individuals to poorer outcomes during respiratory disorders like cystic fibrosis and influenza-associated pneumonia. A common link between these disorders is dysregulation of alveolar fluid clearance via disruption of epithelial sodium channel (ENaC) activity. Recent evidence suggests that female sex hormones directly regulate expression and activity of alveolar ENaC. In our study, we identified the mechanism by which estradiol (E2) or progesterone (P4) independently regulates alveolar ENaC. Using cell-attached patch clamp, we measured ENaC single-channel activity in a rat alveolar cell line (L2) in response to overnight exposure to either E2 or P4. In contrast to P4, E2 increased ENaC channel activity ( NPo) through an increase in channel open probability ( Po) and an increased number of patches with observable channel activity. Apical plasma membrane abundance of the ENaC α-subunit (αENaC) more than doubled in response to E2 as determined by cell surface biotinylation. αENaC membrane abundance was approximately threefold greater in lungs from female rats in proestrus, when serum E2 is greatest, compared with diestrus, when it is lowest. Our results also revealed a significant role for the G protein-coupled estrogen receptor (Gper) to mediate E2's effects on ENaC. Overall, our results demonstrate that E2 signaling through Gper selectively activates alveolar ENaC through an effect on channel gating and channel density, the latter via greater trafficking of channels to the plasma membrane. The results presented herein implicate E2-mediated regulation of alveolar sodium channels in the sex differences observed in the pathogenesis of several pulmonary diseases.

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